*NEW* Schizophrenia: Biological explanations for SZ Flashcards
What is the genetic explanation for sz
It is believed that there is a genetic link between sufferers of SZ, it is therefore passed through families.
Investigated through family studies, twin studies and adoption studies
What did Gottesmann find? (family study)
Found children with two schizophrenic parents = 46% cr , children with one sz parent = 13% and siblings = 9%
What did Joseph find? (twin studies)
MZ = 40.4% and DZ = 7.4%
What did Tiernari find ? (adoption study)
Finland, 164 doptees whose biological mothers had SZ = 11 received a diagnosis compared to 4 of the 197 control group adoptees . Confirms genetic link
What is the dopamine hypothesis for SZ?
claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with positive symptoms.
Explain the dopamine hypothesis
Messages from neurons that transmit dopamine fire too easily or too often , leading to hallucinations and delusions that are characteristic positive symptom of SZ. Abnormally high number D2 receptors on receiving neurons , resulting in more dopamine bindings and therefore more neurons firing
What evidence is there that supports the dopamine hypothesis
- Amphetamine is a dopamine agonist (stimulates dopamine) , ‘normal’ individuals who are exposed to high levels of amphetamine can develop hallucinations and delusions, similarly to a schizophrenic episode .
- Antipsychotics drugs all have one thing in common, they block the activity of dopamine in the brain. Reducing activity in the neural pathways of the brain that use dopamine eliminates hallucinations and delusions. The fact these drugs alleviate many symptoms of SZ demonstrates that dopamine has an important role in this disorder.
What is the revised dopamine hypothesis?
The negative and cognitive symptoms of sz are thought to be caused by a deficit of dopamine in areas of the prefrontal cortex
What evidence is there that supports the revised dopamine hypothesis?
Neural imaging = using PET scans to assess dopamine levels in schizophrenic and normal individuals found lower levels of dopamine in the prefrontal cortex of schizophrenic patients vs normal controls
Animal studies = induced dopamine depletion to the prefrontal cortex in rats. This resulted in cognitive impairment that the researchers reversed using an antipsychotic drug thought to have beneficial effects on negative symptoms in humans.
What are limitations of of the genetic explanation?
- Common rearing patterns may explain family similarities . Many researchers now accept that schizophrenia appears to run in families may be more to do with common rearing patterns that have nothing to do with hereditary
- MZ twins encounter more similar environments . Joseph argues that there is reason to believe the differences in concordance rates between MZ and DZ twins reflect nothing more than environmental differences that distinguish between the two types of twins
- reductionist and deterministic - ‘doomed’ to be schizophrenic
What is a strength of the dopamine hypothesis?
Successful drug treatments which attempt to change dopamine levels in the brain. Leucht et al carried out a meta-analysis of 212 studies that looked into the effectiveness of different antipsychotic drugs compared with a placebo. All drugs tested were significantly more effective than placebo, achieved through the normalisation of dopamine.
Limitation of dopamine hypothesis?
- Noll claims there is strong evidence against both the original and revised dopamine hypothesis. He argues that in antipsychotic drugs do not alleviate hallucinations and delusions in 1/3 of people experiencing these symptoms. In some people hallucinations and delusions are present despite levels of dopamine being normal . Blocking the D2 of these individuals has little or no effect on their symptoms . This suggests that other neurotransmitter systems may also produce the positive symptoms associated with sz.
